Microscopic polyangiitis = hypersensitivity vasculitis = leukocytoclastic vasculitis. Microscopic polyangiitis is a type of small-vessel vasculitis.
There are two main types of small-vessel vasculitis: immune complex (+) and immune complex (-) [pauci immune]. Diseases such as SLE, Henoch-Schönlein purpura, cryoglobulinemia can produce small-vessel vasculitis with immune complexes. Pauci immune small-vessel vasculitis include: (1) Microscopic polyangiitis (-asthma, -granuloma); (2) granulomatosis with polyangiitis (Wegener granulomatosis -apparently, Wegener was a Nazi collaborator and this name is being discouraged-) [-asthma, +granuloma]; (3) Churg-Strauss syndrome (+asthma, -granuloma).
wait, how is it immune complex - if it is c-anca or p-anca positive? this is for the pauci immune
Microscopic polyangiitis = hypersensitivity vasculitis = leukocytoclastic vasculitis. Microscopic polyangiitis is a type of small-vessel vasculitis.
There are two main types of small-vessel vasculitis: immune complex (+) and immune complex (-) [pauci immune]. Diseases such as SLE, Henoch-Schönlein purpura, cryoglobulinemia can produce small-vessel vasculitis with immune complexes. Pauci immune small-vessel vasculitis include: (1) Microscopic polyangiitis (-asthma, -granuloma); (2) granulomatosis with polyangiitis (Wegener granulomatosis -apparently, Wegener was a Nazi collaborator and this name is being discouraged-) [-asthma, +granuloma]; (3) Churg-Strauss syndrome (+asthma, -granuloma).
I'm pretty sure Churg Strauss has granulomatous inflammation.
As far as microscopic polyangiitis, my understanding is it's classified as both pauci-immune and a type III HS reaction, but these seem incompatible to me - are these somehow compatible?
How do antibodies get inside neutrophils to bind to cytoplasmic/perinuclear structures? Antibodies can cross cell membranes?
They can cross the cell membranes of dead cells. So when IF test is performed, antibodies can bind to the cytoplasmic antigens.
You are correct in noting that Churg-Strauss can also have granulomas. However, microscopic polyangiitis is not a type III hypersensitivity reaction (if it were, then it would've been possible to diagnose these lesions using IF of affected tissue). Small-vessel vasculitis with immune complexes is typical for SLE and HSP. Medium-vessel vasculitis with immune complexes is seen in PAN.
What you're saying would be logically consistent. I think microscopic polyangiitis was previously referred to as hypersensitivity angiitis (though I think that's being phased out), and UWorld QID 457 mentioned the etiology as being a type III HS (thus the confusion) usually against penicillin
Unfortunately I don't have a subscription to UW yet, so I can't check it. Do they mention anything else? It doesn't make much sense for microscopic polyangiitis to be a type III hypersensitivity. However, a drug-induced vasculitis can be mediated via immune complexes.
UWorld said:Microscopic polyangiitis (leukocytoclastic or hypersensitivity angiitis) is the most common vasculitis from antibiotic use. Microscopic polyangiitis differs from PAN in that it affects small vessels only. A type III hypersensitivity reaction is the pathogenesis, and the antigen is often a drug (commonly penicillin).
So, while what they've written has some truth to it, saying ''A type III hypersensitivity reaction is the pathogenesis, and the antigen is often a drug'' doesn't sound correct to me, even if we take what is written above into account. Since most lesions are pauci-immune, the main mechanisms should be pauci-immune. Also, Robbins also does not list it among type III hypersensitivities, like I said above.Pathogenesis.
In some cases, an antibody response to antigens such as drugs (e.g., penicillin), microorganisms (e.g., streptococci), heterologous proteins, or tumor proteins has been implicated; this can either result in immune complex deposition or may trigger secondary immune responses (e.g., the development of p-ANCAs) that are ultimately pathogenic.However, most lesions are pauci-immune (devoid of immune complexes), and increasingly, MPO-ANCAs are causally implicated.[68] Recruitment and activation of neutrophils within a particular vascular bed may be responsible for the disease manifestations.
I went back and checked Robbins PBOD. It does not list microscopic polyangiitis among type III hypersensitivities. It does list SLE, post-streptococcal GN, PAN, reactive arthritis, serum sickness and Arthus reaction. However, under the discussion of microscopic polyangiitis, this is written:
So, while what they've written has some truth to it, saying ''A type III hypersensitivity reaction is the pathogenesis, and the antigen is often a drug'' doesn't sound correct to me, even if we take what is written above into account. Since most lesions are pauci-immune, the main mechanisms should be pauci-immune. Also, Robbins also does not list it among type III hypersensitivities, like I said above.
If this were to come up in the real deal, I would stick to pauci-immune.
